Our aim is to elucidate the mechanism of action of insulin and the other hormones on the cellular regulation of glucose metabolism, lipid storage and mobilization and transport of substrates. We will employ fat cells as the model system for its well-known sensitivity to such hormonal influence, especially insulin. Many of the hormones' actions are now understood as mediated by a chain of chemical reactions initiated at the plasma membrane. We have already identified a key step in these reactions, beyond the binding of insulin to its specific receptors, as an electron exchange reaction, involving the oxidation of some membrane sulfhydryls. We recently provided a convincing model showing that such conformational change is facilitatory to the insulin-stimulated glucose transport. Further, we found evidence of an inherent electron-transfer reaction, catalyzed by divalent cations, e.g. Cu ions, generating H2O2 which can mimic the insulin effects on glucose oxidation. We believe, there may be multiple electron-transfer reactions between the hormone-receptor binding and the expression of its effects. Our attention will focus on (1) the identification and characterization of these important sulfhydryl components, (2) the sequence of chemical events, which will answer significant questions on the energy dissipating and conserving processes e.g., glucose oxidation, lipogenesis and facilitated transport etc. BIBLIOGRAPHIC REFERENCES: Mukherjee, S.P. and Lynn, W.S. Glucocorticoid Inhibition of Glucose Utilization by Rat Adipocytes in Relation to Glutathione and Intracellular Redox Potential. Fed. Proc. 34, abstr. #2502. 1975. Mukherjee, S.P. and Lynn, W.S. Differential Control of Glucose Utilization by Rat Adipocytes by the Glycolytic and Pentose Phosphate Shunt Pathways. Modulation by Redox Agents and Adenosine-5'-triphosphate. Manuscript submitted to J. Biol. Chem. 1975.